Why is meat consumption a risk factor for diabetes? Why does there appear to be a stepwise reduction in diabetes rates as meat consumption drops? Instead of avoiding something in meat, it may be that people are getting something protective from plants. Free radicals may be an important trigger for insulin resistance, and antioxidants in plant foods may help. Put people on a plant-based diet, and their antioxidant enzymes shoot up. So not only do plants provide antioxidants, but may boost our own anti-endogenous antioxidant defenses, whereas, on the conventional diabetic diet, they get worse.

In my video, How May Plants Protect Against Diabetes, I discuss how there are phytonutrients in plant foods that may help lower chronic disease prevalence by acting as antioxidants and anti-cancer agents, and by lowering cholesterol and blood sugar. Some, we're now theorizing, may even be lipotropes, which have the capacity to hasten the removal of fat from our liver and other organs, counteracting the inflammatory cascade believed to be directly initiated by saturated-fat-containing foods. Fat in the bloodstream--from the fat on our bodies or the fat we eat--not only causes insulin resistance, but also produces a low-grade inflammation that can contribute to heart disease and non-alcoholic fatty liver disease.

Fiber may also decrease insulin resistance. One of the ways it may do so is by helping to rid the body of excess estrogen. There is strong evidence for a direct role of estrogens in the cause of diabetes, and it's been demonstrated that certain gut bacteria can produce estrogens in our colon. High-fat, low-fiber diets appear to stimulate the metabolic activity of these estrogen-producing intestinal bacteria. This is a problem for men, too. Obesity is associated with low testosterone levels and marked elevations of estrogens produced not only by fat cells but also by some of the bacteria in our gut. Our intestinal bacteria may produce these so-called diabetogens (diabetes-causing compounds) from the fats we eat. By eating lots of fiber, though, we can flush this excess estrogen out of our bodies.

Vegetarian women, for example, excrete two to three times more estrogens in their stools than omnivorous women, which may be why omnivorous women have 50% higher estrogen blood levels. These differences in estrogen metabolism may help explain the lower incidence of diabetes in those eating more plant-based diets, as well as the lower incidence of breast cancer in vegetarian women, who get rid of twice as much estrogen because they get rid of twice as much daily waste in general.

Either way, "[m]eat consumption is consistently associated with diabetes risk. Dietary habits are readily modifiable, but individuals and clinicians will consider dietary changes only if they are aware of the potential benefits of doing so." The identification of meat consumption as a risk factor for diabetes provides helpful guidance that sets the stage for beneficial behavioral changes. Meat consumption is something doctors can easily ask about, and, once identified, at-risk individuals can then be encouraged to familiarize themselves with meatless options.

Why is meat consumption a risk factor for diabetes? Why does there appear to be a stepwise reduction in diabetes rates as meat consumption drops? Instead of avoiding something in meat, it may be that people are getting something protective from plants. Free radicals may be an important trigger for insulin resistance, and antioxidants in plant foods may help. Put people on a plant-based diet, and their antioxidant enzymes shoot up. So not only do plants provide antioxidants, but may boost our own anti-endogenous antioxidant defenses, whereas, on the conventional diabetic diet, they get worse.

In my video, How May Plants Protect Against Diabetes, I discuss how there are phytonutrients in plant foods that may help lower chronic disease prevalence by acting as antioxidants and anti-cancer agents, and by lowering cholesterol and blood sugar. Some, we're now theorizing, may even be lipotropes, which have the capacity to hasten the removal of fat from our liver and other organs, counteracting the inflammatory cascade believed to be directly initiated by saturated-fat-containing foods. Fat in the bloodstream--from the fat on our bodies or the fat we eat--not only causes insulin resistance, but also produces a low-grade inflammation that can contribute to heart disease and non-alcoholic fatty liver disease.

Fiber may also decrease insulin resistance. One of the ways it may do so is by helping to rid the body of excess estrogen. There is strong evidence for a direct role of estrogens in the cause of diabetes, and it's been demonstrated that certain gut bacteria can produce estrogens in our colon. High-fat, low-fiber diets appear to stimulate the metabolic activity of these estrogen-producing intestinal bacteria. This is a problem for men, too. Obesity is associated with low testosterone levels and marked elevations of estrogens produced not only by fat cells but also by some of the bacteria in our gut. Our intestinal bacteria may produce these so-called diabetogens (diabetes-causing compounds) from the fats we eat. By eating lots of fiber, though, we can flush this excess estrogen out of our bodies.

Vegetarian women, for example, excrete two to three times more estrogens in their stools than omnivorous women, which may be why omnivorous women have 50% higher estrogen blood levels. These differences in estrogen metabolism may help explain the lower incidence of diabetes in those eating more plant-based diets, as well as the lower incidence of breast cancer in vegetarian women, who get rid of twice as much estrogen because they get rid of twice as much daily waste in general.

Either way, "[m]eat consumption is consistently associated with diabetes risk. Dietary habits are readily modifiable, but individuals and clinicians will consider dietary changes only if they are aware of the potential benefits of doing so." The identification of meat consumption as a risk factor for diabetes provides helpful guidance that sets the stage for beneficial behavioral changes. Meat consumption is something doctors can easily ask about, and, once identified, at-risk individuals can then be encouraged to familiarize themselves with meatless options.

For the first 90% of our evolution, humans ate diets containing less than a quarter teaspoon of salt a day. Why? Because we ate mostly plants. Since we went millions of years without salt shakers, our bodies evolved into salt-conserving machines, which served us well until we discovered salt could be used to preserve foods. Without refrigeration, this was a big boon to human civilization. Of course, this may have led to a general rise in blood pressure, but does that matter if the alternative is starving to death since all your food rotted away? But where does that leave us now, when we no longer have to live off pickles and jerky? We are genetically programmed to eat ten times less salt than we do now. Even many "low"-salt diets can be considered high-salt diets. That's why it's critical to understand what the concept of "normal" is when it comes to salt.

As I discuss in my video High Blood Pressure May Be a Choice, having a "normal" salt intake can lead to a "normal" blood pressure, which can help us to die from all the "normal" causes, like heart attacks and strokes.

Doctors used to be taught that a "normal" systolic blood pressure (the top number) is approximately 100 plus age. Babies start out with a blood pressure around 95 over 60, but then as we age that 95 can go to 120 by our 20s, then 140 in our 40s, and keep climbing as we age. (140 is the official cut-off above which one technically has high blood pressure.) That was considered normal, since everyone's blood pressure creeps up as we get older. And if that's normal, then heart attacks and strokes are normal too, since risk starts rising once we start getting above the 100 we had as a baby.

If blood pressures over 100 are associated with disease, maybe they should be considered abnormal. Were these elevated blood pressures caused by our abnormally high salt intake--ten times more than what our bodies were designed to handle? Maybe if we ate a natural amount of salt, our blood pressures would not go up with age and we'd be protected. Of course, to test that theory you'd have to find a population in modern times that doesn't use salt, eat processed food, or go out to eat. For that, you'd have to go deep into the Amazon rainforest.

Meet the Yanomamo people, a no-salt culture with the lowest salt intake ever reported. That is, they have a totally normal-for-our-species salt intake. So, what happens to their blood pressure on a no- or low-salt diet as they age? They start out with a blood pressure of about 100 over 60 and end up with a blood pressure of about 100 over 60. Though theirs is described as a salt-deficient diet, that's like saying they have a diet deficient in Twinkies. They're the ones, it seems, who are eating truly normal salt intakes, which leads to truly normal blood pressures. Those in their 50s have the blood pressure of a 20-year-old. What was the percentage of the population tested with high blood pressure? Zero. However, elsewhere in Brazil, up to 38% of the population may be affected. The Yanomamos probably represent the ultimate human example of the importance of salt on blood pressure.

Of course, there could have been other factors. They didn't drink alcohol, ate a high-fiber and plant-based diet, got lots of exercise, and had no obesity. There are a number of plant-based populations eating little salt who experience no rise of blood pressure with age, but how do we know what exactly is to blame? Ideally, we'd do an interventional trial. Imagine if we took people literally dying from out-of-control high blood pressure (so called malignant hypertension) where you go blind from bleeding into your eyes, your kidneys shut down, and your heart fails, and then we withhold from these patients blood pressure medications so their fate is certain death. Then, what if we put them on a Yanomamo level of salt intake--that is, a normal-for-the-human-species salt intake--and, if instead of dying, they walked away cured of their hypertension? That would pretty much seal the deal.

Enter Dr. Walter Kempner and his rice and fruit diet. Patients started with blood pressures of 210 over 140, which dropped down to 80 over 60. Amazing stuff, but how could he ethically withhold all modern blood pressure medications and treat with diet alone? This was back in the 1940s, and the drugs hadn't been invented yet.

His diet wasn't just extremely low salt, though; it was also strictly plant-based and extremely low in fat, protein, and calories. There is no doubt that Kempner's rice diet achieved remarkable results, and Kempner is now remembered as the person who demonstrated, beyond any shadow of doubt, that high blood pressure can often be lowered by a low enough salt diet.

Forty years ago, it was acknowledged that the evidence is very good, if not conclusive, that a low enough reduction of salt in the diet would result in the prevention of essential hypertension (the rising of blood pressure as we age) and its disappearance as a major public health problem. It looks like we knew how to stop this four decades ago. During this time, how many people have died? Today, high blood pressure may kill 400,000 Americans every year--causing a thousand unnecessary deaths every day.

For the first 90% of our evolution, humans ate diets containing less than a quarter teaspoon of salt a day. Why? Because we ate mostly plants. Since we went millions of years without salt shakers, our bodies evolved into salt-conserving machines, which served us well until we discovered salt could be used to preserve foods. Without refrigeration, this was a big boon to human civilization. Of course, this may have led to a general rise in blood pressure, but does that matter if the alternative is starving to death since all your food rotted away? But where does that leave us now, when we no longer have to live off pickles and jerky? We are genetically programmed to eat ten times less salt than we do now. Even many "low"-salt diets can be considered high-salt diets. That's why it's critical to understand what the concept of "normal" is when it comes to salt.

As I discuss in my video High Blood Pressure May Be a Choice, having a "normal" salt intake can lead to a "normal" blood pressure, which can help us to die from all the "normal" causes, like heart attacks and strokes.

Doctors used to be taught that a "normal" systolic blood pressure (the top number) is approximately 100 plus age. Babies start out with a blood pressure around 95 over 60, but then as we age that 95 can go to 120 by our 20s, then 140 in our 40s, and keep climbing as we age. (140 is the official cut-off above which one technically has high blood pressure.) That was considered normal, since everyone's blood pressure creeps up as we get older. And if that's normal, then heart attacks and strokes are normal too, since risk starts rising once we start getting above the 100 we had as a baby.

If blood pressures over 100 are associated with disease, maybe they should be considered abnormal. Were these elevated blood pressures caused by our abnormally high salt intake--ten times more than what our bodies were designed to handle? Maybe if we ate a natural amount of salt, our blood pressures would not go up with age and we'd be protected. Of course, to test that theory you'd have to find a population in modern times that doesn't use salt, eat processed food, or go out to eat. For that, you'd have to go deep into the Amazon rainforest.

Meet the Yanomamo people, a no-salt culture with the lowest salt intake ever reported. That is, they have a totally normal-for-our-species salt intake. So, what happens to their blood pressure on a no- or low-salt diet as they age? They start out with a blood pressure of about 100 over 60 and end up with a blood pressure of about 100 over 60. Though theirs is described as a salt-deficient diet, that's like saying they have a diet deficient in Twinkies. They're the ones, it seems, who are eating truly normal salt intakes, which leads to truly normal blood pressures. Those in their 50s have the blood pressure of a 20-year-old. What was the percentage of the population tested with high blood pressure? Zero. However, elsewhere in Brazil, up to 38% of the population may be affected. The Yanomamos probably represent the ultimate human example of the importance of salt on blood pressure.

Of course, there could have been other factors. They didn't drink alcohol, ate a high-fiber and plant-based diet, got lots of exercise, and had no obesity. There are a number of plant-based populations eating little salt who experience no rise of blood pressure with age, but how do we know what exactly is to blame? Ideally, we'd do an interventional trial. Imagine if we took people literally dying from out-of-control high blood pressure (so called malignant hypertension) where you go blind from bleeding into your eyes, your kidneys shut down, and your heart fails, and then we withhold from these patients blood pressure medications so their fate is certain death. Then, what if we put them on a Yanomamo level of salt intake--that is, a normal-for-the-human-species salt intake--and, if instead of dying, they walked away cured of their hypertension? That would pretty much seal the deal.

Enter Dr. Walter Kempner and his rice and fruit diet. Patients started with blood pressures of 210 over 140, which dropped down to 80 over 60. Amazing stuff, but how could he ethically withhold all modern blood pressure medications and treat with diet alone? This was back in the 1940s, and the drugs hadn't been invented yet.

His diet wasn't just extremely low salt, though; it was also strictly plant-based and extremely low in fat, protein, and calories. There is no doubt that Kempner's rice diet achieved remarkable results, and Kempner is now remembered as the person who demonstrated, beyond any shadow of doubt, that high blood pressure can often be lowered by a low enough salt diet.

Forty years ago, it was acknowledged that the evidence is very good, if not conclusive, that a low enough reduction of salt in the diet would result in the prevention of essential hypertension (the rising of blood pressure as we age) and its disappearance as a major public health problem. It looks like we knew how to stop this four decades ago. During this time, how many people have died? Today, high blood pressure may kill 400,000 Americans every year--causing a thousand unnecessary deaths every day.

A study out of the University of North Carolina found no association between dietary fiber intake and diverticulosis. They compared those who ate the highest amount of fiber, 25 grams, to those who ate the smallest amount, which was three times lower at only 8 grams. Finding no difference in disease rates, researchers concluded that a low-fiber diet was not associated with diverticulosis.

The university sent out a press release entitled: "Diets high in fiber won't protect against diverticulosis." The media picked it up and ran headlines such as "High-fiber diet may not protect against diverticulosis, study finds." It went all over the paleo blogs and even medical journals, publishing such statements as an "important and provocative paper...calls into question" the fiber theory of the development of diverticulosis. Other editorials, though, caught the study's critical flaw. To understand this, let's turn to another dietary deficiency disease: scurvy.

Medical experiments on prisoners at Iowa State Penitentiary showed that clinical signs of scurvy start appearing after just 29 days without vitamin C. Experiments on pacifists during World War II showed that it takes about 10 mg of vitamin C a day to prevent scurvy. Imagine going back a few centuries when they were still trying to figure scurvy out. Dr. James Linde had this radical theory that citrus fruits could cure scurvy. What if an experiment was designed to test this crazy theory, in which sailors were given the juice of either one wedge of lemon or three wedges of lemon each day? If a month later on the high seas there was no difference in scurvy rates, one might see headlines from printing presses touting that a low-vitamin C diet is not associated with scurvy.

Well, a wedge of lemon only yields about 2 mg of vitamin C, and it takes 10 mg to prevent scurvy. They would have been comparing one vitamin C-deficient dose to another vitamin C-deficient dose. No wonder there would be no difference in scurvy rates. We evolved eating so many plants that we likely averaged around 600 mg of vitamin C a day. That's what our bodies are biologically used to getting.

What about fiber? How much fiber are we used to getting? More than 100 grams a day! The highest fiber intake group in the North Carolina study was only eating 25 grams, which is less than the minimum recommended daily allowance of about 32 grams. The subjects didn't even make the minimum! The study compared one fiber-deficient diet to another fiber-deficient diet--no wonder there was no difference in diverticulosis rates.

The African populations with essentially no diverticulosis ate diets consisting in part of very large platefuls of leafy vegetables--similar, perhaps, to what we were eating a few million years ago. They were eating plant-based diets containing 70 to 90 grams of fiber a day. Most vegetarians don't even eat that many whole plant foods, although some do. At least vegetarians tend to hit the minimum mark, and they have less diverticulosis to show for it. A study of 47,000 people confirmed that "[c]onsuming a vegetarian diet and a high intake of dietary fiber were both associated with a lower risk of admission to hospital or death from diverticular disease." They had enough people to tease it out. As you'll see in my video Does Fiber Really Prevent Diverticulosis?, compared to people eating a single serving of meat a day or more, those who ate less than half a serving appeared to have a 16% lower risk and pescatarians (eating no meat except fish) had a risk down around 23%. Both of these results weren't in and of themselves statistically significant, but eating vegetarian was. Vegetarians had 35% lower risk, and those eating strictly plant-based appeared to be at 78% lower risk.

As with all lifestyle interventions, it only works if you do it. High-fiber diets only work if they're actually high in fiber.

People commonly ask Do Vegetarians Get Enough Protein?, but maybe they should be more concerned where everyone else is getting their fiber. Ninety-seven percent of Americans don't even reach the recommended daily minimum.

A study out of the University of North Carolina found no association between dietary fiber intake and diverticulosis. They compared those who ate the highest amount of fiber, 25 grams, to those who ate the smallest amount, which was three times lower at only 8 grams. Finding no difference in disease rates, researchers concluded that a low-fiber diet was not associated with diverticulosis.

The university sent out a press release entitled: "Diets high in fiber won't protect against diverticulosis." The media picked it up and ran headlines such as "High-fiber diet may not protect against diverticulosis, study finds." It went all over the paleo blogs and even medical journals, publishing such statements as an "important and provocative paper...calls into question" the fiber theory of the development of diverticulosis. Other editorials, though, caught the study's critical flaw. To understand this, let's turn to another dietary deficiency disease: scurvy.

Medical experiments on prisoners at Iowa State Penitentiary showed that clinical signs of scurvy start appearing after just 29 days without vitamin C. Experiments on pacifists during World War II showed that it takes about 10 mg of vitamin C a day to prevent scurvy. Imagine going back a few centuries when they were still trying to figure scurvy out. Dr. James Linde had this radical theory that citrus fruits could cure scurvy. What if an experiment was designed to test this crazy theory, in which sailors were given the juice of either one wedge of lemon or three wedges of lemon each day? If a month later on the high seas there was no difference in scurvy rates, one might see headlines from printing presses touting that a low-vitamin C diet is not associated with scurvy.

Well, a wedge of lemon only yields about 2 mg of vitamin C, and it takes 10 mg to prevent scurvy. They would have been comparing one vitamin C-deficient dose to another vitamin C-deficient dose. No wonder there would be no difference in scurvy rates. We evolved eating so many plants that we likely averaged around 600 mg of vitamin C a day. That's what our bodies are biologically used to getting.

What about fiber? How much fiber are we used to getting? More than 100 grams a day! The highest fiber intake group in the North Carolina study was only eating 25 grams, which is less than the minimum recommended daily allowance of about 32 grams. The subjects didn't even make the minimum! The study compared one fiber-deficient diet to another fiber-deficient diet--no wonder there was no difference in diverticulosis rates.

The African populations with essentially no diverticulosis ate diets consisting in part of very large platefuls of leafy vegetables--similar, perhaps, to what we were eating a few million years ago. They were eating plant-based diets containing 70 to 90 grams of fiber a day. Most vegetarians don't even eat that many whole plant foods, although some do. At least vegetarians tend to hit the minimum mark, and they have less diverticulosis to show for it. A study of 47,000 people confirmed that "[c]onsuming a vegetarian diet and a high intake of dietary fiber were both associated with a lower risk of admission to hospital or death from diverticular disease." They had enough people to tease it out. As you'll see in my video Does Fiber Really Prevent Diverticulosis?, compared to people eating a single serving of meat a day or more, those who ate less than half a serving appeared to have a 16% lower risk and pescatarians (eating no meat except fish) had a risk down around 23%. Both of these results weren't in and of themselves statistically significant, but eating vegetarian was. Vegetarians had 35% lower risk, and those eating strictly plant-based appeared to be at 78% lower risk.

As with all lifestyle interventions, it only works if you do it. High-fiber diets only work if they're actually high in fiber.

People commonly ask Do Vegetarians Get Enough Protein?, but maybe they should be more concerned where everyone else is getting their fiber. Ninety-seven percent of Americans don't even reach the recommended daily minimum.

A study out of the University of North Carolina found no association between dietary fiber intake and diverticulosis. They compared those who ate the highest amount of fiber, 25 grams, to those who ate the smallest amount, which was three times lower at only 8 grams. Finding no difference in disease rates, researchers concluded that a low-fiber diet was not associated with diverticulosis.

The university sent out a press release entitled: "Diets high in fiber won't protect against diverticulosis." The media picked it up and ran headlines such as "High-fiber diet may not protect against diverticulosis, study finds." It went all over the paleo blogs and even medical journals, publishing such statements as an "important and provocative paper...calls into question" the fiber theory of the development of diverticulosis. Other editorials, though, caught the study's critical flaw. To understand this, let's turn to another dietary deficiency disease: scurvy.

Medical experiments on prisoners at Iowa State Penitentiary showed that clinical signs of scurvy start appearing after just 29 days without vitamin C. Experiments on pacifists during World War II showed that it takes about 10 mg of vitamin C a day to prevent scurvy. Imagine going back a few centuries when they were still trying to figure scurvy out. Dr. James Linde had this radical theory that citrus fruits could cure scurvy. What if an experiment was designed to test this crazy theory, in which sailors were given the juice of either one wedge of lemon or three wedges of lemon each day? If a month later on the high seas there was no difference in scurvy rates, one might see headlines from printing presses touting that a low-vitamin C diet is not associated with scurvy.

Well, a wedge of lemon only yields about 2 mg of vitamin C, and it takes 10 mg to prevent scurvy. They would have been comparing one vitamin C-deficient dose to another vitamin C-deficient dose. No wonder there would be no difference in scurvy rates. We evolved eating so many plants that we likely averaged around 600 mg of vitamin C a day. That's what our bodies are biologically used to getting.

What about fiber? How much fiber are we used to getting? More than 100 grams a day! The highest fiber intake group in the North Carolina study was only eating 25 grams, which is less than the minimum recommended daily allowance of about 32 grams. The subjects didn't even make the minimum! The study compared one fiber-deficient diet to another fiber-deficient diet--no wonder there was no difference in diverticulosis rates.

The African populations with essentially no diverticulosis ate diets consisting in part of very large platefuls of leafy vegetables--similar, perhaps, to what we were eating a few million years ago. They were eating plant-based diets containing 70 to 90 grams of fiber a day. Most vegetarians don't even eat that many whole plant foods, although some do. At least vegetarians tend to hit the minimum mark, and they have less diverticulosis to show for it. A study of 47,000 people confirmed that "[c]onsuming a vegetarian diet and a high intake of dietary fiber were both associated with a lower risk of admission to hospital or death from diverticular disease." They had enough people to tease it out. As you'll see in my video Does Fiber Really Prevent Diverticulosis?, compared to people eating a single serving of meat a day or more, those who ate less than half a serving appeared to have a 16% lower risk and pescatarians (eating no meat except fish) had a risk down around 23%. Both of these results weren't in and of themselves statistically significant, but eating vegetarian was. Vegetarians had 35% lower risk, and those eating strictly plant-based appeared to be at 78% lower risk.

As with all lifestyle interventions, it only works if you do it. High-fiber diets only work if they're actually high in fiber.

People commonly ask Do Vegetarians Get Enough Protein?, but maybe they should be more concerned where everyone else is getting their fiber. Ninety-seven percent of Americans don't even reach the recommended daily minimum.

Diverticula are out-pouchings of our intestine. Doctors like using a tire analogy: high pressures within the gut can force the intestines to balloon out through weak spots in the intestinal wall like an inner tube poking out through a worn tire tread. You can see what they actually look like in my video, Diverticulosis: When Our Most Common Gut Disorder Hardly Existed. These pockets can become inflamed and infected, and, to carry the tire analogy further, can blow out and spill fecal matter into the abdomen, and lead to death. Symptoms can range from no symptoms at all, to a little cramping and bloating, to "incapacitating pain that is a medical emergency." Nine out of ten people who die from the disease never even knew they had it.

The good news is there may be a way to prevent the disease. Diverticular disease is the most common intestinal disorder, affecting up to 70% of people by age 60. If it's that common, though, is it just an inevitable consequence of aging? No, it's a new disease. In 1907, 25 cases had been reported in the medical literature. Not cases in 25% of people, but 25 cases period. And diverticular disease is kind of hard to miss on autopsy. A hundred years ago, in 1916, it didn't even merit mention in medical and surgical textbooks. The mystery wasn't solved until 1971.

How did a disease that was almost unknown become the most common affliction of the colon in the Western world within one lifespan? Surgeons Painter and Burkitt suggested diverticulosis was a deficiency disease--i.e., a disease caused by a deficiency of fiber. In the late 1800s, roller milling was introduced, further removing fiber from grain, and we started to fill up on other fiber-deficient foods like meat and sugar. A few decades of this and diverticulosis was rampant.

This is what Painter and Burkitt thought was going on: Just as it would be easy to squeeze a lump of butter through a bicycle tube, it's easy to move large, soft, and moist intestinal contents through the gut. In contrast, try squeezing through a lump of tar. When we eat fiber-deficient diets, our feces can become small and firm, and our intestines have to really squeeze down hard to move them along. This buildup of pressure may force out those bulges. Eventually, a low-fiber diet can sometimes lead to the colon literally rupturing itself.

If this theory is true, then populations eating high­-fiber diets would have low rates of diverticulosis. That's exactly what's been found. More than 50% of African Americans in their 50s were found to have diverticulosis, compared to less than 1% in African Africans eating traditional plant-based diets. By less than 1%, we're talking zero out of a series of 2,000 autopsies in South Africa and two out of 4,000 in Uganda. That's about one thousand times lower prevalence.

Diverticula are out-pouchings of our intestine. Doctors like using a tire analogy: high pressures within the gut can force the intestines to balloon out through weak spots in the intestinal wall like an inner tube poking out through a worn tire tread. You can see what they actually look like in my video, Diverticulosis: When Our Most Common Gut Disorder Hardly Existed. These pockets can become inflamed and infected, and, to carry the tire analogy further, can blow out and spill fecal matter into the abdomen, and lead to death. Symptoms can range from no symptoms at all, to a little cramping and bloating, to "incapacitating pain that is a medical emergency." Nine out of ten people who die from the disease never even knew they had it.

The good news is there may be a way to prevent the disease. Diverticular disease is the most common intestinal disorder, affecting up to 70% of people by age 60. If it's that common, though, is it just an inevitable consequence of aging? No, it's a new disease. In 1907, 25 cases had been reported in the medical literature. Not cases in 25% of people, but 25 cases period. And diverticular disease is kind of hard to miss on autopsy. A hundred years ago, in 1916, it didn't even merit mention in medical and surgical textbooks. The mystery wasn't solved until 1971.

How did a disease that was almost unknown become the most common affliction of the colon in the Western world within one lifespan? Surgeons Painter and Burkitt suggested diverticulosis was a deficiency disease--i.e., a disease caused by a deficiency of fiber. In the late 1800s, roller milling was introduced, further removing fiber from grain, and we started to fill up on other fiber-deficient foods like meat and sugar. A few decades of this and diverticulosis was rampant.

This is what Painter and Burkitt thought was going on: Just as it would be easy to squeeze a lump of butter through a bicycle tube, it's easy to move large, soft, and moist intestinal contents through the gut. In contrast, try squeezing through a lump of tar. When we eat fiber-deficient diets, our feces can become small and firm, and our intestines have to really squeeze down hard to move them along. This buildup of pressure may force out those bulges. Eventually, a low-fiber diet can sometimes lead to the colon literally rupturing itself.

If this theory is true, then populations eating high­-fiber diets would have low rates of diverticulosis. That's exactly what's been found. More than 50% of African Americans in their 50s were found to have diverticulosis, compared to less than 1% in African Africans eating traditional plant-based diets. By less than 1%, we're talking zero out of a series of 2,000 autopsies in South Africa and two out of 4,000 in Uganda. That's about one thousand times lower prevalence.

By our seventies, one in five of us will suffer from cognitive impairment. Within five years, half of those cognitively impaired will progress to dementia and death. The earlier we can slow or stop this process, the better.

Although an effective treatment for Alzheimer's disease is unavailable, interventions just to control risk factors could prevent millions of cases. An immense effort has been spent on identifying such risk factors for Alzheimer's and developing treatments to reduce them.

In 1990, a small study of 22 Alzheimer's patients reported high concentrations of homocysteine in their blood. The homocysteine story goes back to 1969 when a Harvard pathologist reported two cases of children, one dating back to 1933, whose brains had turned to mush. They both suffered from extremely rare genetic mutations that led to abnormally high levels of homocysteine in their bodies. Is it possible, he asked, that homocysteine could cause brain damage even in people without genetic defects?

Here we are in the 21st century, and homocysteine is considered "a strong, independent risk factor for the development of dementia and Alzheimer's disease." Having a blood level over 14 (µmol/L) may double our risk. In the Framingham Study, researchers estimate that as many as one in six Alzheimer's cases may be attributable to elevated homocysteine in the blood, which is now thought to play a role in brain damage and cognitive and memory decline. Our body can detoxify homocysteine, though, using three vitamins: folate, vitamin B12, and vitamin B6. So why don't we put them to the test? No matter how many studies find an association between high homocysteinea and cognitive decline, dementia, or Alzheimer's disease, a cause-and-effect role can only be confirmed by interventional studies.

Initially, the results were disappointing. Vitamin supplementation did not seem to work, but the studies were tracking neuropsychological assessments, which are more subjective compared to structural neuroimaging--that is, actually seeing what's happening to the brain. A double-blind randomized controlled trial found that homocysteine-lowering by B vitamins can slow the rate of accelerated brain atrophy in people with mild cognitive impairment. As we age, our brains slowly atrophy, but the shrinking is much accelerated in patients suffering from Alzheimer's disease. An intermediate rate of shrinkage is found in people with mild cognitive impairment. The thinking is if we could slow the rate of brain loss, we may be able to slow the conversion to Alzheimer's disease. Researchers tried giving people B vitamins for two years and found it markedly slowed the rate of brain shrinkage. The rate of atrophy in those with high homocysteine levels was cut in half. A simple, safe treatment can slow the accelerated rate of brain loss.

A follow-up study went further by demonstrating that B-vitamin treatment reduces, by as much as seven-fold, the brain atrophy in the regions specifically vulnerable to the Alzheimer's disease process. You can see the amount of brain atrophy over a two-year period in the placebo group versus the B-vitamin group in my Preventing Brain Loss with B Vitamins? video.

The beneficial effect of B vitamins was confined to those with high homocysteine, indicating a relative deficiency in one of those three vitamins. Wouldn't it be better to not become deficient in the first place? Most people get enough B12 and B6. The reason these folks were stuck at a homocysteine of 11 µmoles per liter is that they probably weren't getting enough folate, which is found concentrated in beans and greens. Ninety-six percent of Americans don't even make the minimum recommended amount of dark green leafy vegetables, which is the same pitiful number who don't eat the minimum recommendation for beans.

If we put people on a healthy diet--a plant-based diet--we can drop their homocysteine levels by 20% in just one week, from around 11 mmoles per liter down to 9 mmoles per liter. The fact that they showed rapid and significant homocysteine lowering without any pills or supplements implies that multiple mechanisms may have been at work. The researchers suggest it may be because of the fiber. Every gram of daily fiber consumption may increase folate levels in the blood nearly 2%, perhaps by boosting vitamin production in the colon by all our friendly gut bacteria. It also could be from the decreased methionine intake.

Methionine is where homocysteine comes from. Homocysteine is a breakdown product of methionine, which comes mostly from animal protein. If we give someone bacon and eggs for breakfast and a steak for dinner, we can get spikes of homocysteine levels in the blood. Thus, decreased methionine intake on a plant-based diet may be another factor contributing to lower, safer homocysteine levels.

The irony is that those who eat plant-based diets long-term, not just at a health spa for a week, have terrible homocysteine levels. Meat-eaters are up at 11 µmoles per liter, but vegetarians at nearly 14 µmoles per liter and vegans at 16 µmoles per liter. Why? The vegetarians and vegans were getting more fiber and folate, but not enough vitamin B12. Most vegans were at risk for suffering from hyperhomocysteinaemia (too much homocysteine in the blood) because most vegans in the study were not supplementing with vitamin B12 or eating vitamin B12-fortified foods, which is critical for anyone eating a plant-based diet. If you take vegans and give them B12, their homocysteine levels can drop down below 5. Why not down to just 11? The reason meat-eaters were stuck up at 11 is presumably because they weren't getting enough folate. Once vegans got enough B12, they could finally fully exploit the benefits of their plant-based diets and come out with the lowest levels of all.